Regulation of Schwann cell function by the extracellular matrix

Chernousov, Michael A.; Yu, Weiming; Chen, Zu-Lin; Carey, David J.; Strickland, Sidney

doi:10.1002/glia.20740

Cited by 167 publications

(146 citation statements)

References 104 publications

(161 reference statements)

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“…The highly differential expression of ECM molecules coincides with axonal growth and the on-going process of Schwann cell precursor migration along the axons, suggesting a potential involvement of such ECM components in these processes. Furthermore, ECM molecules and their receptors have been implicated in Schwann cell development and function (Chernousov et al, 2008), as well as migration (Chernousov et al, 2001;Milner et al, 1997). The ECM protein periostin, which exhibited the most significant differential expression in our microarray analysis, is expressed in a variety of tissues during development, including DRG and Schwann cell precursors, as shown by us and others (Kruzynska-Frejtag et al, 2001;Lindsley et al, 2005).…”

Section: Discussionsupporting

confidence: 67%

Promotion of periostin expression contributes to the migration of Schwann cells

Sonnenberg-Riethmacher

Miehe

Riethmacher

2015

Journal of Cell Science

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Neuregulin ligands and their ErbB receptors are important for the development of Schwann cells, the glial cells of the peripheral nervous system (PNS). ErbB3 deficiency is characterized by a complete loss of Schwann cells along axons of the peripheral nerves, impaired fasciculation and neuronal cell death. We performed comparative gene expression analysis of dorsal root ganglia (DRG) explant cultures from ErbB3-deficient and wild-type mice in order to identify genes that are involved in Schwann cell development and migration. The extracellular matrix (ECM) gene periostin was found to exhibit the most prominent down regulation in ErbB3-deficient DRG. Expression analysis revealed that the periostin-expressing cell population in the PNS corresponds to Schwann cell precursors and Schwann cells, and is particularly high in migratory Schwann cells. Furthermore, stimulation of Schwann cells with neuregulin-1 (NRG1) or transforming growth factor β (TGFβ-1) resulted in an upregulation of periostin expression. Interestingly, DRG explant cultures of periostindeficient mice revealed a significant reduction of the number of migrating Schwann cells. These data demonstrate that the expression of periostin is stimulated by ErbB ligand NRG1 and influences the migration of Schwann cell precursors.

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Section: Discussionsupporting

confidence: 67%

Promotion of periostin expression contributes to the migration of Schwann cells

Sonnenberg-Riethmacher

Miehe

Riethmacher

2015

Journal of Cell Science

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“…The precursor to immature Schwann cell conversion is accompanied by strongly increased proliferation, which is likely to be related to a graded increase in intracellular cAMP controlled by levels of GPR126 (ArthurFarraj et al 2011;Mogha et al 2013), although proliferation falls postnatally during myelination (Stewart et al 1993;Yu et al 2005;Chernousov et al 2008). Proliferation is seldom seen in cells that have segregated to ensheath individual axons and myelinating cells do not divide (Webster et al 1973).…”

Section: What Drives Schwann Cell Proliferation?mentioning

confidence: 99%

Schwann Cells: Development and Role in Nerve Repair

Jessen

Mirsky

Lloyd

2015

Cold Spring Harb Perspect Biol

586

539

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Schwann cells develop from the neural crest in a well-defined sequence of events. This involves the formation of the Schwann cell precursor and immature Schwann cells, followed by the generation of the myelin and nonmyelin (Remak) cells of mature nerves. This review describes the signals that control the embryonic phase of this process and the organogenesis of peripheral nerves. We also discuss the phenotypic plasticity retained by mature Schwann cells, and explain why this unusual feature is central to the striking regenerative potential of the peripheral nervous system (PNS).T he myelin and nonmyelin (Remak) Schwann cells of adult nerves originate from the neural crest in well-defined developmental steps ( Fig. 1). This review focuses on embryonic development (for additional information on myelination, see Salzer 2015). We also discuss how the ability to change between differentiation states, a characteristic attribute of developing cells, is retained by mature Schwann cells, and explain how the ability of Schwann cells to change phenotype in response to injury allows the peripheral nervous system (PNS) to regenerate after damage. TWO TYPES OF EMBRYONIC NERVESAdult nerves are stable structures in which the nerve fibers are protected structurally by a collagen-rich, vascularized extracellular matrix (the endoneurium) linked to the basal lamina surrounding each axon -Schwann cell unit. The endoneurial environment is further protected by a surrounding multilayered cellular tube (the perineurium) that shields the nerve fibers from unwanted cells and molecules (Fig. 2).A more dynamic and radically different structure, reminiscent of axon -glial organization in the central nervous system (CNS), is seen in early embryonic nerves (embryo day E14/15 in rat hind limb and E12/13 in mouse). These nerves consist of tightly packed axons and flattened, glial cell processes without significant extracellular space, matrix, or basal lamina. The glial cell bodies lie among the axons inside the nerve or at the nerve surface. These cells represent the first stage of the Schwann cell lineage, Schwann cell precursors (Figs. 3 and 4).

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“…Thus, MPZ downregulation might be a secondary effect caused by reduced extracellular collagen. Interactions between extracellular matrix components and myelin gene expression have been proposed, although the molecular mechanisms have not been revealed so far (Chen and Strickland, 2003;Chernousov et al, 2006Chernousov et al, , 2008. Alternatively, MPZ downregulation may be a direct effect of reduced ascorbic acid.…”

Section: Discussionmentioning

confidence: 99%

Sodium-Dependent Vitamin C Transporter 2 Deficiency Causes Hypomyelination and Extracellular Matrix Defects in the Peripheral Nervous System

Gess¹,

Röhr²,

Fledrich³

et al. 2011

J. Neurosci.

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Ascorbic acid (vitamin C) is necessary for myelination of Schwann cell/neuron cocultures and has shown beneficial effects in the treatment of a Charcot-Marie-Tooth neuropathy 1A (CMT1A) mouse model. Although clinical studies revealed that ascorbic acid treatment had no impact on CMT1A, it is assumed to have an important function in peripheral nerve myelination and possibly in remyelination. However, the transport pathway of ascorbic acid into peripheral nerves and the mechanism of ascorbic acid function in peripheral nerves in vivo remained unclear.In this study, we used sodium-dependent vitamin C transporter 2-heterozygous (SVCT2 ϩ/Ϫ ) mice to elucidate the functions of SVCT2 and ascorbic acid in the murine peripheral nervous system. SVCT2 and ascorbic acid levels were reduced in SVCT2 ϩ/Ϫ peripheral nerves. Morphometry of sciatic nerve fibers revealed a decrease in myelin thickness and an increase in G-ratios in SVCT2ϩ/Ϫ mice. Nerve conduction velocities and sensorimotor performance in functional tests were reduced in SVCT2 ϩ/Ϫ mice. To investigate the mechanism of ascorbic acid function, we studied the expression of collagens in the extracellular matrix of peripheral nerves. Here, we show that expression of various collagen types was reduced in sciatic nerves of SVCT2 ϩ/Ϫ mice. We found that collagen gene transcription was reduced in SVCT2 ϩ/Ϫ mice but hydroxyproline levels were not, indicating that collagen formation was regulated on the transcriptional and not the posttranslational level. These results help to clarify the transport pathway and mechanism of action of ascorbic acid in the peripheral nervous system and may lead to novel therapeutic approaches to peripheral neuropathies by manipulation of SVCT2 function.

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Regulation of Schwann cell function by the extracellular matrix

Cited by 167 publications

References 104 publications

Promotion of periostin expression contributes to the migration of Schwann cells

Promotion of periostin expression contributes to the migration of Schwann cells

Schwann Cells: Development and Role in Nerve Repair

Sodium-Dependent Vitamin C Transporter 2 Deficiency Causes Hypomyelination and Extracellular Matrix Defects in the Peripheral Nervous System

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